Apolipoprotein E polymorphism in cerebrovascular disease

Objectives– The aim of this study was to investigate the relationship between the apo E genotype with acute cerebral infarction and primary intracerebral haemorrhage and to examine the relationship of the apo E genotype with mortality following acute stroke. Materials and methods– We studied 592 cas...

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Published inActa neurologica Scandinavica Vol. 101; no. 6; pp. 399 - 404
Main Authors Catto, A. J., McCormack, L. J., Mansfield, M. W., Carter, A. M., Bamford, J. M., Robinson, P., Grant, P. J.
Format Journal Article
LanguageEnglish
Published Copenhagen Munksgaard International Publishers 01.06.2000
Blackwell
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Summary:Objectives– The aim of this study was to investigate the relationship between the apo E genotype with acute cerebral infarction and primary intracerebral haemorrhage and to examine the relationship of the apo E genotype with mortality following acute stroke. Materials and methods– We studied 592 cases of acute stroke and 289 healthy control subjects clinically free of cerebrovascular disease. Pathological type of stroke was determined by cranial computed tomography and the subtype of cerebral infarction classified according to the Oxfordshire Community Stroke Project Classification (OCSP). Apo E genotype was determined using polymerase chain reaction. Results– There was no difference in apo E genotype frequency between cases and controls (ξ2=3.58, 5 d.f., P=0.60). Apo E genotypes were not related to the pathological type of stroke (cerebral infarction, CI, n=532 and primary intracranial haemorrhage, PICH, n=60, (ξ2=3.738, 4 d.f., P=0.44) nor with the Oxfordshire Community Stroke Project Classification subtypes of cerebral infarction, lacunar infarction, LACI (n=169), total anterior circulation infarction, TACI (n=117), partial anterior circulation infarction, PACI (n=173), posterior circulation infarction, POCS (n=54) and including those cerebral infarcts which could not be classified (n=19), ξ2=31.1, 20 d.f., P=0.153). At the time of the analysis, 243 cases (41.0%) had died. The median follow‐up (including death) was 851 days. There was no relationship between time to death and apo E genotype in cases of either CI or PICH. Conclusion– In this population, there was no relationship between the apolipoprotein E polymorphism and the pathogenesis of cerebral infarction or primary intracerebral haemorrhage. Apo E genotype was not related to all‐cause mortality following stroke.
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ISSN:0001-6314
1600-0404
DOI:10.1034/j.1600-0404.2000.90308a.x